Apoptosis: A review of pro‐apoptotic and anti‐apoptotic pathways and dysregulation in disease

O'Brien, Mauria; Kirby, Rebecca

doi:10.1111/j.1476-4431.2008.00363.x

Cited by 160 publications

(105 citation statements)

References 164 publications

(214 reference statements)

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“…Apoptotic cells undergo many distinct morphological and biochemical changes (Elmore 2007;O'Brien and Kirby 2008), which lay the foundations for identification of apoptosis. During the early stage of apoptosis, phosphatidylserine (PS) translocates to the outer leaflet of the cell membrane (O'Brien and Kirby 2008;Sgonc and Gruber 1998;Taylor et al 2004;van Engeland et al 1998).…”

Section: Introductionmentioning

confidence: 99%

Quantitative analysis of annexin V–membrane interaction by flow cytometry

Wang

Chen

et al. 2015

Eur Biophys J

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We constructed a green fluorescent phosphatidylserine (PS)-binding probe, which was generated by fusing enhanced green fluorescent protein (EGFP) to the C terminus of human annexin V (anxV). With this probe, we investigated anxV-membrane interaction under different calcium and anxV-EGFP concentrations through flow cytometry (FCM). A mathematical description of the binding characteristics is proposed and validated to quantify the relationship concerning the relative concentration of membrane-bound anxV (B), calcium concentration ([C]), and protein concentration ([P]). Further analyses reveal that [Formula: see text] is linear with [Formula: see text] or [Formula: see text] when [P] and [C] are fixed, respectively, which indicates that the anxV-membrane binding reaction may involve sequential multiple steps. Our study provides a reference for application of anxV in apoptosis detection. The mathematical expression facilitates exploration of the possible interactions between calcium, anxV, and membrane. The corresponding mathematical analysis strengthens the interpretation of the interaction data.

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Section: Introductionmentioning

confidence: 99%

Quantitative analysis of annexin V–membrane interaction by flow cytometry

Wang

Chen

et al. 2015

Eur Biophys J

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“…These receptors have an internal components that mobilize core proteins including TNF receptor-associated death domain (TRADD) and fas-associated death domain (FADD) [11] . Upon binding of the ligand to its receptor, the death-inducing signaling complex (DISC) that causes stimulation of caspase 8 formed [9] . Thusly, caspase 8 activate the remaining downstream caspase enzymes.…”

Section: Mechanisms Of Apoptosismentioning

confidence: 99%

“…The intrinsic and extrinsic apoptotic pathways come together at caspase-3, which splits the inhibitor of the caspase-activated deoxyribonuclease, and the caspase-activated deoxyribonuclease causes nuclear apoptosis. The triggered enzymes cleave regulatory and structural molecules, ending in the death of the cell [9] . Caspases also disturb the cytoskeletal structure, cell cycle and signaling process, eventually leading to the morphological indicators of apoptosis, for instance, DNA condensation and disintegration, and membrane blebbing [4] .…”

Section: Mechanisms Of Apoptosismentioning

confidence: 99%

“…Caspases are initiated by three separate pathways: The intrinsic (or mitochondrial), the extrinsic (or death receptor) and the intrinsic endoplasmic reticulum pathways [9] . The extrinsic pathway is initiated by triggering cell death receptors on the cell surface which leads to activation of the intracellular apoptotic machinery.…”

Section: Mechanisms Of Apoptosismentioning

confidence: 99%

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Apoptotic pathways as a therapeutic target for colorectal cancer treatment

Abraha

Ketema

2016

WJGO

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Colorectal cancer is the second leading cause of death from cancer among adults. The disease begins as a benign adenomatous polyp, which develops into an advanced adenoma with high-grade dysplasia and then progresses to an invasive cancer. Appropriate apoptotic signaling is fundamentally important to preserve a healthy balance between cell death and cell survival and in maintaining genome integrity. Evasion of apoptotic pathway has been established as a prominent hallmark of several cancers. During colorectal cancer development, the balance between the rates of cell growth and apoptosis that maintains intestinal epithelial cell homeostasis gets progressively disturbed. Evidences are increasingly available to support the hypothesis that failure of apoptosis may be an important factor in the evolution of colorectal cancer and its poor response to chemotherapy and radiation. The other reason for targeting apoptotic pathway in the treatment of cancer is based on the observation that this process is deregulated in cancer cells but not in normal cells. As a result, colorectal cancer therapies designed to stimulate apoptosis in target cells would play a critical role in controlling its development and progression. A better understanding of the apoptotic signaling pathways, and the mechanisms by which cancer cells evade apoptotic death might lead to effective therapeutic strategies to inhibit cancer cell proliferation with minimal toxicity and high responses to chemotherapy. In this review, we analyzed the current understanding and future promises of apoptotic pathways as a therapeutic target in colorectal cancer treatment.

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“…Apoptosis is made up of two major pathways called the death receptor pathway and the mitochondrial pathway, which are both propagated by a caspase cascade that ultimately leads to apoptosis induction [27,34]. Evasion of apoptosis during carcinogenesis occurs by three distinct mechanisms: disrupted signalling of death receptors, loss of caspase activity as well as impaired balance between anti-apoptotic and pro-apoptotic proteins [14,42,50,59]. Targeting the caspase cascade, Bcl-2 family proteins as well as other factors associated with apoptosis signalling have thus become the major strategy in anticancer therapeutics (table 1).…”

Section: Targeting Apoptosis In Breast Cancer Treatmentmentioning

confidence: 99%

Apoptotic Molecular Advances in Breast Cancer Management

Moela¹,

Motadi²

2015

Cell Death - Autophagy, Apoptosis and Necrosis

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Breast cancer is the most common cancer type amongst women, accounting for most female cancer deaths second to cervical cancer worldwide. It is, therefore, highly crucial to understand the molecular biology and explore other pathways involved in carcinogenesis in order to select appropriate treatment not only for breast cancer but for other cancers as well. Cancer progression is favoured by DNA damage and in most cases a consequent disruption of the apoptotic pathway, thus leading to uncontrolled cell proliferation. Therefore, current therapeutic strategies aim at targeting the apoptotic pathways in order to combat cancer. In this manuscript, we discuss the ways in which evasion of apoptosis during carcinogenesis occurs and the types of current therapeutic strategies as well as promising future approaches against breast cancer.

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Apoptosis: A review of pro‐apoptotic and anti‐apoptotic pathways and dysregulation in disease

Abstract: Objective -To review the human and veterinary literature on the biology of apoptosis in health and disease.

Cited by 160 publications

References 164 publications

Quantitative analysis of annexin V–membrane interaction by flow cytometry

Quantitative analysis of annexin V–membrane interaction by flow cytometry

Apoptotic pathways as a therapeutic target for colorectal cancer treatment

Apoptotic Molecular Advances in Breast Cancer Management

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